The finding that blood and muscle lactate concentrations are lower during maximal exercise than at sea level has been termed the "lactate paradox (of high altitude)". There are 2 additional components of this paradox that are seldom considered: (i) the cause(s) of fatigue at high altitude which cannot be due to low blood (and muscle) lactate concentrations and (ii) the paradoxically low cardiac outputs that occur even though myocardial function is highly preserved during maximal exercise in extreme hypoxia. Recent studies indicate that exercise in extreme hypoxia occurs at lower levels of ìperipheralî fatigue than during exercise in normoxia or mild hypoxia and must therefore be regulated by the central nervous system. Accordingly the following hypothesis would explain all three components of the lactate paradox: The allowable extent of skeletal muscle recruitment during ìmaximal exerciseî falls progressively with increasing altitude perhaps as a function of the adequacy of cerebral oxygenation. As a result, progressively lower levels of skeletal muscle recruitment prevent the development of sufficient muscle power, leading to the termination of ìmaximalî exercise at progressively lower work rates, cardiac outputs and blood and muscle lactate concentrations with increasing altitude. This control would protect the brain from dangerous levels of hypoxia at extreme altitude.